Temporal enhancement of renin-aldosterone blockade by enalapril, an angiotensin-converting enzyme inhibitor

Publisher Website
Google Scholar
Abstract
Interruption of the renin-aldosterone system with angiotensin-converting enzyme inhibitors (CEI) should result in a low aldosterone secretion, but aldosterone production has generally been measured by plasma aldosterone (PA) levels or urinary metabolites. The effects of CEI of the aldosterone secretion rate (ASR) were evaluated and compared with PA, urinary tetrahydroaldosterone (THA), plasma renin activity (PRA) and electrolyte balance in 6 normotensive subjects in a metabolic unit during a control period (5 days) and during administration of 10 mg/day enalopril for 28 days. The ASR did not decline until after 1 wk of CEI therapy and this was reflected by a corresponding decline in the urine K:Na ratio. Upright PA levels at day 1 declined, but supine PA levels were unchanged. THA excretion remained essentially unchanged and the THA:ASR ratio rose progressively during therapy. PRA rose and was maximal on day 3, but subsequently declined. Enalapril-induced hypoaldosteronism required several days to become demonstrable and this was not accurately assessed by PA or THA, possibly due in part to altered aldosterone metabolism. The simultaneous decline in both PRA and ASR could be due to a decrease in renin substrate. Caution is warranted when assessing aldosterone secretion indirectly by either PA levels or urinary metabolites during CEI therapy.